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Published on: May 28, 2019
Relationship between TRAIL and Left Ventricular Ejection Fraction in Patients with ST-Elevation Myocardial Infarction
Elena Teringova1, Martin Kozel1, Jiri Knot1
1Cardiocenter, Department of Cardiology, 3rd Faculty of Medicine, Charles University and University Hospital Kralovske Vinohrady, Prague, Czech Republic.
Insights
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) levels decrease after reperfusion in ST-elevation myocardial infarction (STEMI) patients. Lower TRAIL is linked to worse left ventricular ejection fraction (LVEF), suggesting TRAIL is protective.
Area of Science:
- Cardiology
- Biochemistry
- Cell Biology
Background:
- Apoptosis is crucial in myocardial injury post-acute myocardial infarction (AMI) and subsequent heart failure development.
- Understanding apoptotic markers aids in managing cardiac function after AMI.
Purpose of the Study:
- To investigate the serum kinetics of TRAIL and sFas in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (pPCI).
- To determine the relationship between TRAIL, sFas levels, and left ventricular ejection fraction (LVEF) post-STEMI.
Main Methods:
- Serum TRAIL and sFas levels were measured in 101 STEMI patients during hospitalization and one month post-pPCI.
- Left ventricular ejection fraction (LVEF) was assessed at admission and one month.
- Major adverse cardiovascular events (MACE) were tracked over a two-year follow-up.
Main Results:
- TRAIL levels decreased post-pPCI, then increased, correlating positively with LVEF at baseline and one month.
- sFas levels were lowest at admission, peaking at one month, and did not correlate with LVEF.
- Neither TRAIL nor sFas predicted LVEF improvement or 2-year MACE.
Conclusions:
- In STEMI patients treated with pPCI, TRAIL serum concentration is lowest after reperfusion.
- Low TRAIL levels are associated with poorer LVEF, both acutely and one month post-STEMI.
- Higher TRAIL levels appear beneficial, indicating TRAIL may be a protective mediator against post-AMI injury.
Background:
Apoptosis plays an important role in the myocardial injury after acute myocardial infarction and in the subsequent development of heart failure.
Aim:
To clarify serum kinetics of apoptotic markers TRAIL and sFas and their relation to left ventricular ejection fraction (LVEF) in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI).
Methods:
In 101 patients with STEMI treated with pPCI, levels of TRAIL and sFas were measured in series of serum samples obtained during hospitalization and one month after STEMI. LVEF was assessed at admission and at one month. Major adverse cardiovascular events (MACE, i.e., death, re-MI, and hospitalization for heart failure and stroke) were analysed during a two-year followup.
Results:
Serum level of TRAIL significantly decreased one day after pPCI (50.5pg/mL) compared to admission (56.7pg/mL), subsequently increased on day 2 after pPCI (58.8pg/mL), and reached its highest level at one month (70.3pg/mL). TRAIL levels on days 1 and 2 showed a significant inverse correlation with troponin and a significant positive correlation with LVEF at baseline. Moreover, TRAIL correlated significantly with LVEF one month after STEMI (day 1: r=0.402, p<0.001; day 2: r=0.542, p<0.001). On the contrary, sFas level was significantly lowest at admission (5073pg/mL), increased one day after pPCI (6370pg/mL), and decreased on day 2 (5548pg/mL). Significantly highest sFas level was marked at one month (7024pg/mL). sFas failed to correlate with LVEF at baseline or at one month. Both TRAIL and sFas showed no ability to predict improvement of LVEF one month after STEMI or a 2-year MACE (represented by 3.29%).
Conclusion:
In STEMI treated with pPCI, TRAIL reaches its lowest serum concentration after reperfusion. Low TRAIL level is associated with worse LVEF in the acute phase of STEMI as well as one month after STEMI. Higher TRAIL level appears to be beneficial and thus TRAIL seems to represent a protective mediator of post-AMI injury.
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